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1 Divisions of Geriatrics and Nutritional Science, Washington University School of Meidicne, St. Louis, MO, USA
2 Endocrinology, Diabetes and Lipid Research and the Center for Human Nutrition, Washington University School of Medicine, St. Louis, MO, USA
3 Divisions of Geriatrics and Nutritional Science, Washington University School of Meidicne, St. Louis, MO, USA; Istituto Superiore di Sanita, Rome, Italy
4 Department of Medicine and Therapeutics, University College, Dblin, Ireland
* To whom correspondence should be addressed. E-mail: dreeds{at}im.wustl.edu.
Dyslipidemia is common in patients with HIV infection. In this study, a two-stage euglycemic, hyperinsulinemic clamp, with infusion of stable isotopically labeled tracers, was used to evaluate insulin action in skeletal muscle, liver and adipose tissue in HIV-infected men with dyslipidemia (HIV-DL; plasma triglyceride >250mg/dl and HDL<45mg/dl; n=12), HIV-infected men without dyslipidemia (HIV w/o DL; n=12), and healthy men (n=6). Basal rates of glucose production (glucose Ra), glucose disposal (glucose Rd), and lipolysis (palmitate Ra) were similar between groups. The relative suppression of glucose Ra (63±4%, 77±2%, and 78±3%; P=0.008) and palmitate Ra (49±4%, 63±3%, and 68±3%; P=0.005) during low-dose insulin infusion (plasma insulin=30 µU/ml), and the relative stimulation of glucose Rd (214±21%, 390±25% and 393±46%; P=0.001) during high-dose insulin infusion (plasma insulin=75µU/ml) were lower in HIV-DL than in HIV w/o DL and healthy volunteers, respectively. Suppression of basal glucose Ra correlated with plasma adiponectin (r =0.44, P=0.02), and inversely with plasma interleukin-6 (r =-0.49, P<0.001). Stimulation of glucose Rd correlated directly with adiponectin (r=0.48, P<0.01) and inversely with IL-6 (r=-0.49, P=0.02). We conclude that dyslipidemia in HIV-infected men is indicative of multi-organ insulin resistance, and circulating adipokines may be important in the pathogenesis of impaired insulin action.
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